Allergic airways diseases such as asthma and allergic rhinitis are of major, and increasing, public health concern, especially in industrialised nations where they represent the most common chronic disorders in children. Asthma, in particular, is a chronic respiratory disorder that has increased alarmingly in prevalence in the last 20 years. Australia has one of the highest rates of asthma in the world, with estimates suggesting that up to 10-20% of the population are affected. Worldwide up to one in four children, one in seven adolescents and one in ten adults will experience symptoms of asthma at some time in their life. In addition to being potentially debilitating for sufferers, the direct and indirect costs of allergic airways diseases on health systems are substantial. In the United States it has been estimated that the direct cost of asthma to the economy is in the order of $15 billion annually, with direct medication costs accounting for about $3 billion of this.
There is a clear need not only for effective therapies for the treatment and management of allergic airways diseases, but also for strategies and approaches to prevent the onset and development of such diseases.
Asthma is an inflammatory disorder causing variability of airflow obstruction, and an increased sensitivity and exaggerated response to many different stimuli (airway hyperresponsiveness), particularly allergens. Together these patho-physiological manifestations lead to symptoms including wheezing, coughing, chest tightness and dyspnoea. The chronic inflammatory response in asthma is characterised by an intense eosinophil infiltrate into the airways and mucous secreting cell hyperplasia that is coordinated by cytokine release from T-helper type 2 (Th2) lymphocytes. Eosinophils release a range of both preformed and newly synthesised mediators that damage the mucosal epithelial lining and promote an exaggerated repair response resulting in tissue remodeling and sub-epithelial fibrosis.
It has been noted that the prevalence of asthma varies inversely with the prevalence of certain bacterial infections such as tuberculosis and typhoid (see for example Jones et al., 2000). These infections, together with those of Mycobacterium Bovis elicit a T-helper type 1 (Th1) immune response, which, during the early years of life, may cause immune deviation from the neonatal Th2 response to a mature Th1 response. The absence of exposure to Th1 inducing infections is thought to promote the persistence of a Th2 phenotype and permits the development of allergy and asthma.
The increasing prevalence of allergic airways diseases, and the increasingly early onset of diseases such as asthma in children, has focused much attention on the need for effective treatments and preventative measures. Whilst research continues, to date there has yet to emerge any effective means of preventing the onset or development of allergic airways diseases such as asthma.